Improving the performance of thermophilic anaerobic digester through recirculation of low hydrogen biogas.

Biogas recirculation was conducted to improve the performance of two thermophilic anaerobic sequenced batch reactors (ASBRs), in which high concentrations of volatile fatty acids (VFAs) were accumulated. To accelerate degradation of VFAs, facilitating acetate consumption via syntrophic acetate oxidation coupled with hydrogenotrophic methanogenesis (SAO-HM) was expected to be effective. Hence, to promote the SAO-HM pathway, hydrogen was removed to create low hydrogen partial pressure (pH2) in reactor RH, yet in reactor RB, hydrogen was not treated. The performance of RB and RH on VFAs degradation and methane production processes was compared at steady stage; the VFAs and soluble microbial products (SMP) in the effluents were monitored. The results showed that low pH2 intensified the SAO reaction, thereby accelerating conversion of acetate to methane, as well as acetate production from glucose and VFAs. Glucose fermentation type was also influenced. VFAs and SMP in the effluents were reduced after the introduction of biogas mixing, which proceeded much faster in RH with low pH2. Recirculation of low hydrogen biogas with SAO-HM pathway being promoted should be more effective to alleviate high acid level stress and to improve the reactor performance.

Effect of excessive iodine exposure on the placental deiodinase activities and Hoxc8 expression during mouse embryogenesis.

Excessive iodine induces thyroid dysfunction. However, the effect of excessive iodine exposure on maternal-fetal thyroid hormone metabolism and on the expression of genes involved in differentiation, growth and development is poorly understood. Since a thyroid hormone receptor response element was found in the Hoxc8 promoter region, Hoxc8 expression possibly regulated by excessive iodine exposure was firstly investigated. In the present study, Balb/C mice were given different doses of iodine in the form of potassium iodate (KIO3) at the levels of 0 (sterile water), 1.5, 3.0, 6.0, 12.0 and 24.0 microg/ml in drinking water for 4 months, then were mated. On 12.5 d postcoitum, placental type 2 and type 3 deiodinase activities and fetal Hoxc8 expression were determined. The results showed that excessive iodine exposure above 1.5 microg/ml resulted in an increase of total thyroxine and a decrease of total triiodothyronine in the serum of maternal mice, which was mainly associated with the inhibition of type 1 deiodinase activity in liver and kidney. Placental type 2 deiodinase activity decreased, showing an inverse relationship with maternal thyroxine level. Hoxc8 mRNA and protein expression at 12.5 d postcoitum embryos were down regulated. Because Hoxc8 plays an important role in normal skeletal development, this finding provides a possible explanation for the skeletal malformation induced by excessive iodine exposure and also provides a new clue to study the relationship between iodine or thyroid hormones and Hox gene expression pattern.

Developmental toxic effects of chronic exposure to high doses of iodine in the mouse.

Chronic exposure to high doses of iodine induces thyroid dysfunction, but effects of chronic exposure to high amounts of iodine on pregnancy and fetal outcome are uncertain. In the present study, Balb/C mice were given different doses of iodine at the levels of 0 (sterile water), 1,500, 3,000, 6,000, 12,000 and 24,000 micro g/L in drinking water for 4 months, then were mated and the developmental toxicity and teratogenicity were evaluated. An obvious colloid goiter was observed, and serum total thyroxine (TT4) levels increased and serum total triiodothyronine (TT3) levels decreased significantly in dams when iodine dose reached 3,000 micro g/L. Maternal effect was evident by the reduction of average daily food consumption in higher doses of iodine groups. Embryotoxicity and teratogenicity were mainly indicated by the reduced body weight in female fetuses, the decreased number of live fetuses, and the increased incidence of resorptions, and especially skeletal variations. These results suggest that exposure to maternally toxic doses of iodine may have a potential developmental toxic effect.